Suppression of a high-affinity transport system for manganese in cadmium-resistant metallothionein-null cells

J Pharmacol Exp Ther. 2000 Mar;292(3):1080-6.

Abstract

Cadmium is a hazardous heavy metal existing ubiquitously in the environment, but the mechanism of cadmium transport into mammalian cells has been poorly understood. Recently, we have established a cadmium-resistant cell line (Cd-rB5) from immortalized metallothionein-null mouse cells, and found that Cd-rB5 cells exhibited a marked decrease in cadmium uptake. To investigate the mechanism of altered uptake of cadmium in Cd-rB5 cells, incorporation of various metals was determined simultaneously using a multitracer technique. Cd-rB5 cells exhibited a marked decrease in manganese incorporation as well as that of cadmium. However, the reduced uptake of manganese was observed only at low concentrations, suggesting that a high-affinity component of the Mn(2+) transport system was suppressed in Cd-rB5 cells. Competition experiments and kinetic analyses revealed that low concentrations of Cd(2+) and Mn(2+) share the same high-affinity pathway for their entry into cells. The mutual competition of Cd(2+) and Mn(2+) uptake was also observed in HeLa, PC12, and Caco-2 cells. The highest uptake of Cd(2+) and Mn(2+) by parental cells occurred at neutral pH, suggesting that this pathway is different from a divalent metal transporter 1 that can transport various divalent metals including Cd(2+) and Mn(2+) under acidic conditions. These results suggest that a high-affinity Mn(2+) transport system is used for mammalian cellular cadmium uptake, and that the suppression of this pathway caused a marked decrease in cadmium accumulation in cadmium-resistant metallothionein-null cells.

MeSH terms

  • Animals
  • Biological Transport
  • Cadmium / metabolism*
  • Cell Line
  • Drug Resistance
  • Hydrogen-Ion Concentration
  • Manganese / metabolism*
  • Metallothionein / physiology*
  • Mice

Substances

  • Cadmium
  • Manganese
  • Metallothionein